Elsevier

Seminars in Perinatology

Volume 30, Issue 4, August 2006, Pages 179-184
Seminars in Perinatology

Pathology of Bronchopulmonary Dysplasia

https://doi.org/10.1053/j.semperi.2006.05.004Get rights and content

Over the past three decades, advances in prenatal and neonatal intensive care have contributed to marked improvements in survival rates for extremely immature infants born during the canalicular phase of lung development at 24 to 26 weeks, a time when alveolar and distal vascular development is rapidly occurring. The histopathological lesions of severe airway injury and alternating sites of overinflation and fibrosis in “old” BPD have been replaced in “new” BPD with the pathologic changes of large, simplified alveolar structures, a dysmorphic capillary configuration, and variable interstitial cellularity and/or fibroproliferation. Airway and vascular lesions, when present, tend to be present in infants, who over time develop more severe disease. The concept that “new” BPD results in an arrest in alveolization should be modified to that of an impairment in alveolization as evidence shows that short ventilatory times and/or the use of nCPAP allow continued alveolar formation.

Section snippets

Similarities/Differences in the Pathology of Animal Models of BPD in Relation to Human BPD

Bronchopulmonary dysplasia is the end result of lung injury in a developmentally immature host, so developmental similarities should exist between the animal model and the human disease. The immature infant will breathe some level of oxygen, and even room air represents a hyperoxic exposure. Because ventilator-induced lung injury plays a significant role in the pathogenesis of BPD, studies would require that volutrauma or biotrauma be mechanistically examined. The presence of a predelivery

Acknowledgement

This work is supported in part by NIH Grant HL52636.

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